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Blocking NAD(+)/CD38/cADPR/Ca(2+) pathway in sepsis prevents organ damage
Qian-Yi Peng1, Mei-Lin Ai1, Li-Na Zhang1
1Department of Critical Care Medicine, Xiang-Ya Hospital, Central South University, Changsha, Hunan Province, China.
The Journal of Surgical Research
|March 30, 2016
Summary
The nicotinamide adenine dinucleotide (NAD(+))/CD38/cyclic ADP ribose (cADPR)/Ca(2+) pathway activates during sepsis. Inhibiting this pathway with 8-Br-cADPR protects organs from sepsis-induced damage, offering a potential therapeutic target.
Area of Science:
- Biochemistry
- Cellular Signaling
- Pathophysiology
Background:
- The NAD(+)/CD38/cADPR/Ca(2+) pathway regulates calcium homeostasis and inflammation.
- Its role in sepsis pathophysiology is currently unknown.
Purpose of the Study:
- To investigate the activation of the NAD(+)/CD38/cADPR/Ca(2+) pathway in sepsis.
- To evaluate the protective effects of the inhibitor 8-Br-cADPR against sepsis-induced organ damage.
Main Methods:
- Rats underwent cecal ligation and puncture (CLP) to induce sepsis.
- NAD(+), cADPR, CD38, and intracellular Ca(2+) levels were measured in organs.
- Tissue injury, malondialdehyde, and superoxide dismutase activity were assessed in CLP and CLP+8-Br-cADPR groups.
Main Results:
- Sepsis led to increased NAD(+), cADPR, CD38, and intracellular Ca(2+) levels in heart, liver, and kidney tissues.
- 8-Br-cADPR treatment inhibited Ca(2+) mobilization and attenuated tissue injury.
- Treatment reduced malondialdehyde and increased superoxide dismutase activity in septic rats.
Conclusions:
- The NAD(+)/CD38/cADPR/Ca(2+) signaling pathway is activated during sepsis.
- Inhibition of this pathway with 8-Br-cADPR demonstrates organ protective effects in a sepsis model.
